One of the postulated mechanisms of Sudden Infant Death has been increase in respiratory load. We believe that respiratory load compensating mechanisms in adults may be under-developed in infancy. Adults respond to loads by an immediate increase in the impedance of the respiratory system which stabilises the tidal volume. This is due to the intrinsic properties of the chest wall and diaphragm. The chest wall in infancy is so compliant that the same volume stabilisation by this mechanism is unlikely. Furthermore, an adult responds to an elastic load by increasing respiratory rate. In neonates and probably some infants the Hering Beuer reflex is active, and will cause a decrease in respiratory rate if the tidal volume is reduced. Thus loads which are trivial for an adult may cause a disastrous fall in minute volume in infancy. Chemoreceptor compensation is relatively ineffective when the respiratory system is loaded. We therefore propose to test the hypothesis that compensation for respiratory loads is not developed in some infants and that this may contribute to apnoea in the premature infant and to the Sudden Infant Death Syndrome.